In this study, we focused on patients with malignant tumors of stomach, lung and breast, and defined the Abnormal Hilit types of 343 tumor patients, as Abnormal Khan, Pleghem, Sapra and Savda, by dialectical diagnosis based on the Hilit pathology theory of TUM. We further classified tumor patients into two groups according to Abnormal Hilit types, as Abnormal Savda type tumor (ASt) and non-Abnormal Savda type tumor (nASt), which includes patients with other three Abnormal Hilits. We studied the changes in regulatory networks of plasma protein expression shared by different malignant tumor patients with ASt compared to nASt by application of iTRAQ-based plasma proteomics, bioinformatics and quantitative validation. As a result, we identified 31 plasma proteins as common candidate markers for ASt by setting more than 1.2 times of quantitative differences as standard for comparative analysis. Meanwhile, we established a clinical therapeutic evaluation model (patients) through treatment of patients with ASt by prescribing the specific prescriptions for Abnormal Savda, the Abnormal Savda Munziq and the Abnormal Savda Mushil, according to the theories of TUM, “the disease coupled with a syndrome” and “a prescription corresponding to a syndrome”, and identified 27 plasma proteins as potential therapeutic targets of the prescription by proteomics analysis. In addition, by comparative analysis of both potential protein marker profiles common to ASt and influenced by the treatment of ASt with the prescriptions, we showed that the treatment of Abnormal Savda type tumors by the prescriptions may directly regulate or recover the plasma levels of at least 5 proteins altered with the development of Abnormal Savda type tumors. Among them, the upregulation of von Willebrand factor, Thrombospondin 1 and Insulin-like growth factor-binding protein and the downregulation of fibrinogen and inter-alpha-trypsin inhibitor heavy chain H3 in Abnormal Savda syndrome were inversely regulated by clinical treatment with the prescriptions.